Dual channel implantation neurostimulation techniques

ABSTRACT

A first electrical signal and a second electrical signal are transmitted to one or more implanted leads including first and second electrodes, respectively. The first and second signals have a difference in frequency such that the combined potentials induce action potentials in a certain locus of electrically excitable tissue. Means are provided for adjusting the frequency difference, as well as the amplitudes of the signals so that the locus is altered.

BACKGROUND OF THE INVENTION

1. Field of the Invention

This invention relates to means of stimulating electrically excitabletissue, and more particularly relates to means for adjusting the locusat which action potentials are induced in such tissue.

2. Description of the Related Art

Two major practical problems reduce the efficacy of epidural spinal cordstimulation (SCS) for pain control. One is the difficulty of directingthe stimulation-induced paresthesia to the desired body part and theother is the problem of disagreeable sensations or motor responses tothe stimulation, which reduce the comfortable amplitude range of thestimulation. It is generally agreed that in SCS, for chronic pain,paresthesia should cover the whole pain region. With present stimulationmethods and equipment, only highly skilled and experienced practitionersare able to position a stimulation lead in such a way that the desiredoverlap is reached and desired results are obtained over time withminimal side effects. It requires much time and effort to focus thestimulation on the desired body region during surgery and, with singlechannel approaches, it is difficult to redirect it afterwards, eventhough some readjustments can be made by selecting a different contactcombination, pulse rate, pulse width or voltage.

Redirecting paresthesia after surgery is highly desirable. Even ifparesthesia covers the pain area perfectly during surgery, the requiredparesthesia pattern often changes later due to lead migration, orhistological changes (such as the growth of connective tissue around thestimulation electrode) or disease progression. The problem of leadplacement has been addressed by U.S. Pat. No. 5,121,754 by the use of alead with a deformable distal shape. These problems are not only foundwith SCS, but also with peripheral nerve stimulation (PNS), depth brainstimulation (DBS), cortical stimulation and also muscle or cardiacstimulation.

A system capable of some adjustment of spinal cord excitation isdescribed in PCT International Publication No. WO 95/19804. However,that system requires three electrodes, optimally spaced, which is aserious handicap during the surgical procedure required in order toplace these electrodes in the body. Three electrodes may require the useof a paddle arrangement which is surgically difficult to manipulateadjacent the spinal cord. In addition, that system has only limitedadjustment capability, dependent on the distance from the electrodes tothe spinal cord.

SUMMARY OF THE INVENTION

The present invention can be used to advantage for altering the locus inelectrically excitable tissue at which action potentials are induced.According to a preferred embodiment, first and second electrodes areimplanted adjacent the tissue to be stimulated. A first electricalsignal is applied to the first electrode and a second electrical signalis applied to the second electrode. The frequency difference between thefirst and second signals is adjusted and the amplitudes of the first andsecond signals are adjusted such that the combined potentials induced inthe locus by the first and second signals create action potentials inthe locus, and the locus is altered.

By using the foregoing techniques, the degree of surgical precisionrequired for the implanting of the electrodes is reduced, because thelocus at which the nerve fibers are stimulated can be adjusted by merelychanging the frequency difference and amplitudes of the signals appliedto the electrodes after the surgical procedure is completed.

According to another embodiment of the invention, the signals may beeither sinusoidal or pulsed.

BRIEF DESCRIPTION OF THE DRAWINGS

These and other advantages and features of the invention will becomeapparent upon reading the following detailed description and referringto the accompanying drawings in which like numbers refer to like partsthroughout and in which:

FIG. 1 is a diagrammatic view of a patient in which a preferred form ofapparatus for spinal cord stimulation (SCS) made in accordance with theinvention has been implanted;

FIG. 2 is a cross-sectional view of an exemplary spinal column showing atypical position at which electrodes made in accordance with thepreferred practice of the invention have been implanted in the epiduralspace;

FIG. 3 is a cross-sectional view like FIG. 2 showing locus of potentialchanges induced in the spinal cord from a signal applied to a first oneof two electrodes;

FIG. 4 is a view like FIG. 3 showing the locus of potential changesinduced in the spinal cord from the application of a signal to thesecond of the electrodes;

FIG. 5 is a view like FIG. 4 showing the combined loci in the spinalcord at which potentials are induced from signals applied to the firstand second electrodes;

FIG. 6 is a view like FIG. 5 showing the alteration of the loci due toincrease in the amplitude of the signal applied to the first electrodeand a decrease in amplitude of the signal applied to the secondelectrode;

FIG. 7 is a view like FIG. 6 showing the alteration of the loci due toan increase in amplitude of the signal applied to the second electrodeand a decrease in amplitude of the signal applied to the firstelectrode; and

FIG. 8 is a timing diagram showing signals applied to the first andsecond electrodes illustrated in FIG. 2 in relationship to thepotentials induced in tissue adjacent the electrodes.

FIG. 9 depicts an idealistic representation of the dual channel ITREL("DCI") version of the implantable pulse generator utilized in one ofthe preferred embodiments of the present invention.

FIG. 10 shows the monolithic embodiment of switches N1 and N2 of FIG. 9along with the additional circuitry required to actuate or toggle eachswitch into the closed or open position.

FIGS. 11A-D is a schematic of the electrode switch utilized in eachstimulating ("S"), recharging ("R"), and stimulating or recharging ("Sor R") switch depicted in FIG. 9.

FIG. 12 is a schematic of the circuit used to identify the most negativereference that is utilized as the AMP₋₋ OUT voltage level of FIG. 9.

FIGS. 13 and 14A-E illustrate the top level representation--along withthe relevant control signals driving the electrode switches--of theoutput circuit depicted in FIG. 9.

FIGS. 15A-15I, 16A-B, 17, 18, 19, 20, 21A-D, and 22A-C illustrate analternative output circuit configuration for the implantable pulsegenerator. This alternative output circuit is called "transversetripolar stimulation."

DESCRIPTION OF THE PREFERRED EMBODIMENTS

Referring to FIG. 8, a single electrical signal or pulse, such as P1,can cause depolarization near a cathode in electrically excitable tissuewhich includes neural tissue and muscle tissue. Neural tissue includesperipheral nerves, the spinal cord surface, deep spinal cord tissue,deep brain tissue, and brain surface tissue. Muscle tissue includesskeletal (red) muscle, smooth (white) muscle, and cardiac muscle. Alocus includes a set of points in three-dimensional space and refers toa volume of cells or parts of cells. Due to the electricalcharacteristics of both the three-dimensional volume conductor and themembrane properties, the potentials outside and inside a neuron respondto the depolarization, usually with exponential-type increases and thenattenuation over time. The time constant for an isolated neuron membranetypically is 5-15 milliseconds (Nerve, Muscle and Synapse by BernardKatz, circa 1972). For myelinated axons or muscle cells, it may beconsiderably shorter.

As shown in FIG. 8, the local depolarization from a single pulse P1results in a transmembrane potential PT1 between times T1 and T3. Thepeak of potential PT1 is below the transmembrane potential thresholdTPT. As a result, the pulse fails to produce an action potential in thatcell.

Action potential is an all-or-none, nonlinear phenomenon, caused byopening of sodium gates, inrush of sodium of ions, and a delayed openingof potassium gates and a restoration of the membrane potential. Ingeneral, a certain amount of charge must be passed at the electrodes(amplitude Volts!/ resistance Ohms!×pulse width time!) in order to causeenough depolarization for an action potential to begin. There is areciprocal relationship between amplitude and pulse width: the productmust reach a certain value before the threshold is reached. Thisrelationship does not reach the Volts=0 axis. There is a certain minimumvoltage needed, called rheobase, before an action potential can happen.

Basic neurophysiological principles, called "electrotonus", show that inany volume of electrically excitable tissue in which two or more pulses,each of which alone is insufficient to bring the cells to threshold,arrive closely together in time, at least part of their effect isadditive, i.e., the memory of the first pulse is still present when thesecond pulse arrives. If the sum of the potentials (distorted byresistive and capacitive properties of the surroundings and the cellmembranes) can get some cells depolarized to threshold, then an actionpotential will start in those cells.

Still referring to FIG. 8, the inducement of an action potential in acell is illustrated by a transmembrane depolarizing potential PT3reaching the transmembrane potential threshold TPT at time T4.

FIG. 1 is a schematic view of a patient 10 having an implant of aneurological stimulation system employing a preferred form of thepresent invention to stimulate spinal cord 12 of the patient. Thepreferred system employs an implantable pulse generator 14 to produce anumber of independent stimulation pulses which are sent to spinal cord12 by insulated leads 16 and 18 coupled to the spinal cord by electrodes16A and 18A (FIG. 2). Electrodes 16A and 18A also can be attached toseparate conductors included within a single lead.

In the preferred embodiment, implantable pulse generator 14 is either amodified ITREL II or a dual channel ITREL ("DCI"). Both models of theseimplantable pulse generators are commercially available from Medtronic,Inc. and are capable of delivering multiple signals to the one or moreelectrodes on different channels. The implantable pulse generator 14 canprovide multiple signals at different adjustable frequencies, pulsewidths, amplitudes, and repetition rates. However, in the DCIimplantable pulse generator 14, the repetition rates on the differentchannels are synchronized. The detailed configuration of the outputcircuitry utilized in the DCI implantable pulse generator 14 is shown inFIGS. 9-14.

The idealistic representation of the DCI version of the implantablepulse generator 14 is depicted in FIG. 9. In this version of theimplantable pulse generator 14, the pulse widths are digitallycontrolled by a timer. The implantable pulse generator 14 must be ableto generate different amplitudes while preventing unwantedcross-conduction from occurring between different electrode switchesduring stimulation. In this version of the implantable pulse generator14, only one of the channels of electrode switches are stimulated at anygiven time by the implantable pulse generator 14.

The programmed amplitude of the signal output of each channel of the DCIimplantable pulse generator 14 is stored across two differentcapacitors, C2 and C3. These capacitors C2 and C3 are commonlyreferenced to the same node AMP₋₋ OUT. Therefore, AMP1 and AMP2represent the two amplitudes (voltages) that are stored acrosscapacitors C2 and C3. The 183 ohm resistor and switch 52 is used todischarge all or a portion of the charge on capacitors C2 and C3,thereby reducing the stored amplitude(s). Similarly, the switchingregulator 50 is used to increase the charge, and thus amplitude, oncapacitors C2 and C3.

Thus, in order to use the electrodes (TPE) on channel 1 ("CH1") orchannel 2 ("CH2") to stimulate the biological load or tissue "RL",switches N1 or N2 must first be respectively opened or closed. Afterswitch N1 or N2 is closed, the tissue "RL" is stimulated when thestimulating switches (designated "S") or the stimulating/rechargingswitches (designated "S or R") are closed. After the stimulation pulseis complete, the system then waits a finite period of time beforeproducing a recharging pulse. In the preferred embodiment, the finiteperiod of time is 244 μsec.; however, a delay of 100 to 500 μsec. couldbe used. After the finite period of time elapses, the rechargingswitches (designated "R") or the "S or R" switches are closed in orderto reverse the current through the tissue "RL", or in other words torecharge the tissue. The reason for the finite period of time delay isto prevent the physiological cancellation of the stimulation effect. Thedetailed circuit configuration of the "S", "R", and "S or R" monolithicswitches can be seen in FIG. 11.

Other than capacitors C2 and C3, the capacitors 54 depicted in FIG. 9are used to maintain charge balance. Similarly, capacitors can beinstalled between the following terminal pairs in order to maintaincharge balance: CPB1₋₋ 1--CPB1₋₋ 2 and CPB2₋₋ 1--CPB2₋₋ 2.

As previously mentioned, FIGS. 15-22 illustrate an alternative outputcircuit configuration for the implantable pulse generator 14 called"transverse tripolar stimulation." This circuit configuration allowsboth channels to be utilized in order to simultaneously providedifferent amplitudes, frequencies, repetition rates, and pulse widths tothree electrodes (one reference electrode and two electrodes atdifferent amplitudes).

In the preferred embodiment of the present invention, the system employsa programmer 20 which is coupled via a conductor 22 to a radio frequencyantenna 24. This system permits attending medical personnel to selectthe various signal output options--such as amplitude, pulse width,frequency, and repetition rate--after implant using radio frequencycommunications. While the preferred system employs fully implantedelements, systems employing partially implanted generators andradio-frequency coupling may also be used in the practice of the presentinvention (e.g., similar to products sold by Medtronic, Inc. under thetrademarks X-trel and Mattrix).

FIG. 2 is a cross-sectional view of spine 12 showing implantation of thedistal end of insulated leads 16 and 18 which terminate in electrodes16A and 18A within epidural space 26. The electrodes may be conventionalpercutaneous electrodes, such as PISCES® model 3487A sold by Medtronic,Inc. Also shown is the subdural space 28 filled with cerebrospinal fluid(cfs), bony vertebral body 30, vertebral arch 31, and dura mater 32. Thespine also includes gray matter 34 and dorsal horns 36 and 37 and whitematter, for example, dorsal columns 46 and dorsal lateral columns 47.

Referring to FIG. 8, signal P1 is applied to electrode 18A (FIG. 2) andsignal P2 is applied to electrode 16A (FIG. 2). Although signals P1 andP2 are shown as pulses, they also may comprises sinusoidal signals.Pulses P1 and P2 are generated at different frequencies. When theelectric fields resulting from P1 and P2 pass through the same point inspace at different frequencies, there is a difference frequency electricfield set up corresponding to the difference between the frequencies ofthe two signals. For example, if P1 is generated at 150 Hz and P2 isgenerated at 50 Hz, the resulting difference frequency will be 100 Hzwhich is in the physiologic range.

Amplitude A1 of P1 is adjustable independently from amplitude A2 of P2.For the case in which amplitudes A1 and A2 are equal, the amplitude ofthe resulting difference frequency electric field is twice the amplitudeof the individual electric fields.

Referring to FIG. 3, line L1 represents the edge of a three-dimensionallocus L1A in which pulse P1 applied to electrode 18A induces a potentialPT1 between times T1 and T3 that is less than the transmembranepotential threshold TPT for cells of interest in that locus.

Referring to FIG. 4, line L2 represents the edge of anotherthree-dimensional locus L2A in which the application of pulse P2 (FIG.8) to electrode 16A induces a depolarizing potential less than thetransmembrane potential threshold TPT for cells of interest in thatlocus.

FIG. 5 illustrates a locus L3A representing the intersection of loci L1Aand L2A in which the combined potentials induced in locus L3A from thedifference frequency electric field produced by pulses P1 and P2 createsan action potential in cells of interest in locus L3A as illustrated bypotential PT3 in FIG. 8. The potential induced in locus L1A outsidelocus L3A is illustrated by potential PT1 (FIG. 8). Since PT1 is lowerthan the transmembrane potential threshold TPT, there is no actionpotential created in locus L1A outside L3A. The potential created inlocus in L2A outside L3A is illustrated by potential PT2 (FIG. 8). Sincepotential PT2 is less than the transmembrane potential threshold TPT,there is no action potential created in locus L2A outside locus L3A.

Referring to FIG. 6, line L4 represents the edge of anotherthree-dimensional locus L4A resulting from the application of a pulse P1to electrode 18A having an amplitude greater than amplitude A1 (FIG. 8),and line L5 represents the edge of another three-dimensional locus L5Aresulting from the application of a pulse P2 to electrode 16A having anamplitude less than amplitude A2. The intersection of loci L4A and L5Arepresents a locus L6A resulting from the difference frequency electricfield produced by pulses P1 and P2 in which action potentials areinduced. Locus L6A is moved mostly to the right relative to locus L3Ashown in FIG. 5. Action potentials are not induced outside locus L6A.

Referring to FIG. 7, line L8 represents the edge of anotherthree-dimensional locus L8A resulting from the application of a pulse P2to electrode 16A having an amplitude greater than amplitude A2 (FIG. 8),and line L7 represents the edge of another three-dimensional locus L7Aresulting from the application of a pulse P1 to electrode 18A having anamplitude less than amplitude A1. The intersection of loci L7A and L8Arepresents a locus L9A resulting from the difference frequency electricfield produced by pulses P1 and P2 in which action potentials areinduced. It will be noted that the locus L9A is moved to the leftcompared with locus L3A shown in FIG. 5. Action potentials are notinduced outside locus L9A.

The ability to move the locus in which action potentials are induced isan important feature. In many therapies, it is important to preventaction potentials being induced in gray matter 34 or dorsal horns 36 and37, dorsal roots 38 and 40, dorsal lateral columns 47 or peripheralnerves 42 and 44 in order to minimize the possibility of causing pain,motor effects, or uncomfortable paresthesia. In the describedtechniques, the locus in which action potentials are induced (e.g., L3A,L6A or L9A) can be manipulated to a desired area of the dorsal columns46 without inducing action potentials in dorsal horns 36 and 37, graymatter 34 or dorsal lateral columns 47. Moreover, the ability to movethe locus in which action potentials are induced drastically reduces theaccuracy necessary for surgically implanting electrodes 16A and 18A, andmay eliminate the need for surgical lead revisions.

The foregoing techniques also may be applied to all electricallyexcitable tissue. Those skilled in the art will recognize that thepreferred embodiments may be altered and amended without departing fromthe true spirit and scope of the appended claims.

We claim:
 1. A system for altering the locus of electrically excitabletissue in which action potentials are induced comprising incombination:a first electrode adapted to be implanted adjacent saidtissue; a second electrode adapted to be implanted adjacent said tissue;means for applying a first electrical signal having a first frequencyand first amplitude to said first electrode and a second electricalsignal having a second frequency and second amplitude to said secondelectrode, the frequency difference between said first frequency andsaid second frequency having a relationship such that the combinedpotentials induced in said locus by said first and second signals createaction potentials in said locus; and means for adjusting said first andsecond frequencies and said first and second amplitudes so that saidlocus is altered.
 2. A system, as claimed in claim 1, wherein said meansfor adjusting comprises means for making said first and secondamplitudes substantially identical.
 3. A system, as claimed in claim 1,wherein said first and second signals comprise sinusoidal signals.
 4. Asystem, as claimed in claim 1, wherein said first and second signalscomprise pulse signals.
 5. A method for altering the locus ofelectrically excitable tissue in which action potentials are induced bymeans of first and second electrodes adapted to be implanted adjacentsaid tissue, said method comprising the steps of:applying a firstperiodic electrical signal to said first electrode; applying a secondperiodic electrical signal to said second electrode; adjusting thedifference in frequency between said first and second signals; andadjusting the amplitudes of said first and second signals, such that thelocus of the combined potentials induced by said first and secondsignals in which action potentials are created is altered, whereby thelocus is positioned with respect to said tissue.
 6. A method, as claimedin claim 5, wherein the step of adjusting said amplitudes comprises thestep of making said amplitudes substantially identical.
 7. A method, asclaimed in claim 5, using sinusoidal signals for said first and secondsignals.
 8. A method, as claimed in claim 5, using pulse signals forsaid first and second signals.